A transversion from T to A in the second base of the only Vps25 intron causes a splicing defect and, subsequently, premature termination of translation by an in-frame stop codon in the intron.
Nucleotide substitution: T29A.
T8625577A
T29A
T to A mutation in the second base of the intron.
abnormal size | adult stage (with Vps25N55)
eye | somatic clone (with Vps25N55)
Vps25N55/Vps25K2 mosaic eyes are larger than wild-type, even if homozygous mutant clones are not recovered, indicating that the mutant clones do not contribute to the adult eye tissue, but appear to be able to induce overgrowth in wild-type tissue. Third-instar eye-antennal discs are overgrown and disorganised when compared with wild-type.
TUNEL labelling, indicating the beginning of apoptosis, is increased in Vps25K2 mutant clones, consistent with the lack of mutant clones in the adult eye. Vps25K2 clones can grow to a fairly large size, suggesting that they are not growth-impaired. However, these clones are completely removed by apoptosis during pupal stages.
Vps25K2 is a suppressor of increased cell death phenotype of hidGMR.PG
Vps25N55/Vps25K2 is a suppressor of eye | somatic clone | cell non-autonomous phenotype of hidGMR.PG
Vps25K2 is rescued by Vps25UAS.cHa
Vps25K2 is rescued by Vps25hs.PH